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Therefore, the unphysiological state of high circulating melatonin levels concurrent with food intake, as seen in nocturnally feeding populations, shift-workers or users of exogenous melatonin, may result in dysregulation of glucose metabolism and contribute to an increased risk of T2D development (20). They proposed a so-called “timing model,” in which they describe that low melatonin during eating periods supports high glucose tolerance, while high melatonin during fasting could facilitate β-cell recovery (20). It has been hypothesized that the link between disturbed sleep and metabolic changes could be mediated by perturbations in eating behaviors, including increased energy intake, as well as higher frequency and number of meals and snacks consumed per day (17). Disturbed sleep alters metabolic pathways and contributes to insulin resistance, as well as deregulation of energy expenditure and appetite, contributing to an increased disease risk. 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